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Basic Pathology > Plasma Protein Systems, Cytokines, and Inflammation Outcomes > Flashcards

Plasma Protein Systems, Cytokines, and Inflammation Outcomes Flashcards

1
Q

plasma protein systems

A

free floating proteins found in the blood, produced by the liver in a steady state during normal times, ramped up during inflammation; enzymatic cascades allow for amplification of immune response; all systems interact and also have regulatory components to turn it off

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2
Q

complement system

A
  • triggered by 3 different pathways
  • inflammation amplifier
  • attacks pathogens
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3
Q

3 pathways of complement system

A
  • classical pathway
  • alternative pathway
  • lectin pathway
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4
Q

classical pathway

A
  • initiated by antigen:antibody complex

- activates C1 complex to start cascade

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5
Q

lectin pathway

A
  • similar to classical pathway

- initiated by mannose-binding lectin (MBL)

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6
Q

alternative pathway

A
  • initiated by pathogen antigens

- binds free-floating C3b to create C3 Convertase

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7
Q

complement cascade products

A
  • C3a and C5a
  • C3b
  • C5b + C6-C9
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8
Q

C3a and C5a

A
  • anaphylotoxins (cause mast cell degranulation)

- chemotactic factors (leaves trail for leukocytes to follow to where they’re needed)

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9
Q

C3b

A

opsonins (tags pathogen for removal)

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10
Q

C5b + C6-C9

A

membrane attack complex (MAC)

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11
Q

C3b attaches to _____; ___ recognize opsonins

A

bacteria surfaces; phagocytes

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12
Q

membrane attack complex (MAC)

A

complement proteins insert themselves into the membrane of pathogens, creating pores; water and ions enter the cell; cell swells and lyses

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13
Q

complement system deficiencies: activation disorders

A

hard time turning it on; recurrent infections

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14
Q

complement system deficiencies: inhibitory disorders

A

hard time turning it off; ex: hereditary angioedema

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15
Q

coagulation system is activated by ____

A

endothelial damage and bleeding

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16
Q

coagulation system: intrinsic pathway is triggered by ___

A

vascular damage and platelets

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17
Q

coagulation system: extrinsic pathway is triggered by ___

A

external damage and tissue factor

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18
Q

coagulation system: intrinsic and extrinsic pathways share ____

A

final pathway

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19
Q

coagulation system forms a ____, which ____

A

fibrinous meshwork; prevents hemorrhage, traps pathogens, and prepares for repair

20
Q

coagulation system contributes to ____

A

inflammation (activates kinin and complement systems)

21
Q

kinin system is activated by ____

A

bleeding

22
Q

kinin system is ____

A

pro-inflammatory

23
Q

product of kinin system is ____, which ____

A

bradykinin;
is similar to histamine; causes vasodilation, pain, smooth muscle contraction, increases vascular permeability, and leukocyte chemotaxis

24
Q

cytokines are soluble factors produced by ____

A

cellular mediators of inflammation and injured cells

25
Q

there are many types of cytokines, the 3 main ones we focused on are ____

A

interleukins, interferon, and tumor necrosis factor-a

26
Q

cytokines are pleiotropic, meaning ___

A

the effect depends on which cells are activated; development, maturation, localization, and activation of immune cells

27
Q

cytokines have ____ targets

A

local and distant

28
Q

interleukins

A
  • macrophage and lymphocyte product
  • chemotactic
  • activates adaptive immune response (i.e., lymphocytes)
  • > 30 types
29
Q

IL-1

A

endogenous pyrogen, chemotaxis, leukocytosis, pro-inflammatory

30
Q

IL-10

A

inhibits lymphocyte growth and macrophage activity, anti-inflammatory

31
Q

interferon

A
  • produced by virus-infected cells, macrophages, and lymphocytes
  • induces non-specific antiviral response and increases macrophage activity
32
Q

tumor necrosis factor-a

A
  • produced by macrophages and mast cells in response to PAMPs
  • increases endothelial adhesion molecules and macrophage activity
33
Q

short term effects of tumor necrosis factor-a

A

induces fever (endogenous pyrogen) and increases PPS (plasma protein system) production

34
Q

long term effects of tumor necrosis factor-a

A

promotes cachexia (wasting) and intravascular thrombosis (clotting throughout body)

35
Q

termination of inflammation

A
  • removal of an offending agent usually ends response

- checks exist to control course of inflammation

36
Q

checks exist to control course of inflammation:

A
  • neutrophil lifespan is short
  • inflammatory mediators degrade rapidly
  • anti-inflammatory cytokines are also produced
37
Q

4 outcomes of acute inflammation

A

1) complete resolution
2) scarring
3) abscess formation
4) progression to chronic formation

38
Q

complete resolution

A

structure and function recoverable

39
Q

scarring

A

substantial damage to connective tissue

40
Q

abscess formation

A

pus confined in a closed space; active proteases produce a fluid, increasing pressure; usually must drain

41
Q

progression to chronic inflammation

A

body cannot remove offending agent; persistent bacteria/toxins or autoimmune diseases

42
Q

chronic inflammation

A
  • inflammation lasting 2 weeks or longer

- often related to an unsuccessful acute inflammatory response

43
Q

causes of chronic inflammation

A
  • high lipid wax content of microorganism (tuberculosis)
  • ability to survive inside the macrophage (chlamydia)
  • toxins and chemical irritants (alcohol abuse)
  • physical limitations (punctual plug)
  • particulate matter (asbestos, soot, etc.)
44
Q

chronic inflammation has a dense infiltration of ____

A

lymphocytes and macrophages (also fibroblasts)

45
Q

chronic inflammation has fibrosis, which is ____

A

thickening and scarring of connective tissue (collagen)

46
Q

chronic inflammation has angiogenesis, which is ____

A

production of new blood vessels (VEGF)

47
Q

chronic inflammation has granuloma formation, which is ____

A

walling off of the offending agent with collagen

Basic Pathology (21 decks)

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